Noda M, Rodan G A
Department of Bone Biology and Osteoporosis Research, Merck, Sharp, & Dohme Research Laboratories, West Point, Pennsylvania 19486.
J Cell Biol. 1989 Feb;108(2):713-8. doi: 10.1083/jcb.108.2.713.
Osteopontin (OP) or bone sialoprotein is a recently characterized extracellular matrix protein which is abundant in bone and is produced by osteoblasts. Parathyroid hormone (PTH) is a potent calcitropic hormone which regulates osteoblastic function including the synthesis of extracellular matrix proteins. This study examines the effect of human PTH (hPTH-[1-34]) on the expression of this novel protein in rat osteoblast-like cells. hPTH(1-34) significantly decreased the amount of OP in culture media of the rat osteoblastic osteosarcoma cell line, ROS 17/2.8, detected by Western immunoblot analysis. hPTH(1-34) also suppressed the steady-state level of OP mRNA two- to threefold with an ED50 of approximately 3 X 10(-10) M. This inhibition was detectable at 24 h, reached its nadir at 48 h, and lasted at least up to 96 h. The hPTH(1-34) effects were mimicked by isobutylmethylxanthine, cholera toxin, 8-bromo-cAMP, forskolin, and isoproterenol. hPTH(1-34) suppressed by two- to threefold the rate of OP gene transcription, estimated by nuclear run-on assays. The suppression of OP mRNA levels by hPTH(1-34) was also seen when basal levels were increased by transforming growth factor type beta, or 1,25-dihydroxyvitamin D3, or were decreased by dexamethasone. A similar decrease in the steady-state level of OP mRNA by hPTH(1-34) was also observed in primary cultures of osteoblast-enriched cells from fetal rat calvaria. These findings indicate that hPTH(1-34) suppresses the production of the novel extracellular matrix protein, OP, in osteoblasts at least in part through transcriptional control.
骨桥蛋白(OP)或骨唾液蛋白是一种最近被鉴定的细胞外基质蛋白,在骨中含量丰富,由成骨细胞产生。甲状旁腺激素(PTH)是一种有效的钙调节激素,可调节成骨细胞功能,包括细胞外基质蛋白的合成。本研究检测了人PTH(hPTH-[1-34])对大鼠成骨样细胞中这种新蛋白表达的影响。通过Western免疫印迹分析检测,hPTH(1-34)显著降低了大鼠成骨样骨肉瘤细胞系ROS 17/2.8培养基中OP的含量。hPTH(1-34)还使OP mRNA的稳态水平降低了两到三倍,半数有效剂量(ED50)约为3×10(-10) M。这种抑制在24小时时可检测到,在48小时时达到最低点,并至少持续到96小时。异丁基甲基黄嘌呤、霍乱毒素、8-溴-cAMP、福斯可林和异丙肾上腺素可模拟hPTH(1-34)的作用。通过核转录分析估计,hPTH(1-34)使OP基因转录速率降低了两到三倍。当基础水平通过转化生长因子β型、1,25-二羟基维生素D3升高或通过地塞米松降低时,hPTH(1-34)也能抑制OP mRNA水平。在来自胎鼠颅骨的富含成骨细胞的原代培养物中,也观察到hPTH(1-34)使OP mRNA的稳态水平有类似下降。这些发现表明,hPTH(1-34)至少部分通过转录控制抑制成骨细胞中新型细胞外基质蛋白OP的产生。